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Memories and recursion to the mean

The behavioral data revealed that as the rat awaited the second stimulus of the trial, the memory of the first stimulus shifted towards the mean of preceding stimuli.
The experiment thus confirmed the sliding of memory towards the expected value, a phenomenon that earlier studies have termed 'contraction bias.'

Neurons get the beat and keep it going in drumrolls -- ScienceDaily

The researchers recorded the activities of individual neurons in the hippocampus, which is located in the lower center of the brain, with a robotic device called a patch clamp. It's a hollow glass needle one micron in diameter that latches onto a single neuron via suction and measures its electrical activity.
The researchers observed electrical rumblings, symbolized here by a drumroll. And they observed spikes, symbolized here by a cymbal crash.
Though the pattern of rumblings wasn't uniform, it rose and fell like a drumroll undulating between softer and louder volumes. Spikes occurred much more rarely than drumbeats, but with notable timing.
"The spikes repeated in the same spots with high precision, so they weren't just random," Singer said. "They came around the peaks of rumblings, not always right on top of a peak but within a hair of it."
It would be like a cymbal crash hitting not every time, but every few times the undulating drumroll topped a volume peak. And the drumroll-cymbal-crash patterns sustained themselves for surprisingly long periods.
"The time periods of activity that was structured like this were much longer than we expected," Singer said. "People have shown sustained periods of signaling like this for 100 to 300 milliseconds before, but this appears to be the first time it's been seen for 900 milliseconds (nearly a full second), and it may go on even longer."

Midbrain 'start neurons' control whether we walk or run -- ScienceDaily

The researchers identify populations of 'start neurons' and show, for the first time, how the two regions in the midbrain can act both in common or separately to control speed and to select context dependent locomotor behaviours.
"By identifying the midbrain 'start' neurons we complement a previous study where we found 'stop cells' in the brainstem that halt locomotion. Together, the start and stop cells define the episodic nature of locomotion," says Ole Kiehn.
The study breaks new grounds in locomotor control and is important for understanding the normal brain function in mice. And the authors believe that the results might benefit humans with disabled locomotion as well.

Neurons aren't binary

In an article published today in the journal Scientific Reports, the researchers go against conventional wisdom to show that each neuron functions as a collection of excitable elements, where each excitable element is sensitive to the directionality of the origin of the input signal. Two weak inputs from different directions (e.g., "left" and "right") will not sum up to generate a spike, while a strong input from "left" will generate a different spike waveform than that from the "right."
"We reached this conclusion using a new experimental setup, but in principle these results could have been discovered using technology that has existed since the 1980s. The belief that has been rooted in the scientific world for 100 years resulted in this delay of several decades," said Prof. Kanter and his team of researchers, including Shira Sardi, Roni Vardi, Anton Sheinin, and Amir Goldental.

Some video games are good for older adults' brains -- ScienceDaily

"3-D video games engage the hippocampus into creating a cognitive map, or a mental representation, of the virtual environment that the brain is exploring.," said West. "Several studies suggest stimulation of the hippocampus increases both functional activity and gray matter within this region."
Conversely, when the brain is not learning new things, gray matter atrophies as people age. "The good news is that we can reverse those effects and increase volume by learning something new, and games like Super Mario 64, which activate the hippocampus, seem to hold some potential in that respect," said West. Added Belleville: "These findings can also be used to drive future research on Alzheimer's, since there is a link between the volume of the hippocampus and the risk of developing the disease."

hronic alcohol abuse results in alcohol-related neurodegeneration, and critical gaps in our knowledge hinder therapeutic development. Neural stem cells (NSCs) are a subpopulation of cells within the adult brain that contribute to brain maintenance and recovery. While it is known that alcohol alters NSCs, little is known about how NSC response to alcohol is related to sex, brain region, and stage of differentiation. Understanding these relationships will aid in therapeutic development. Here, we used an inducible transgenic mouse model to track the stages of differentiation of adult endogenous NSCs and observed distinct NSC behaviors in three brain regions (subventricular zone, subgranular zone, and tanycyte layer) after long-term alcohol consumption. Particularly, chronic alcohol consumption profoundly affected the survival of NSCs in the subventricular zone and altered NSC differentiation in all three regions. Significant differences between male and female mice were further discovered.

Your brain does not process information and it is not a computer | Aeon Essays

Worse still, even if we had the ability to take a snapshot of all of the brain’s 86 billion neurons and then to simulate the state of those neurons in a computer, that vast pattern would mean nothing outside the body of the brain that produced it. This is perhaps the most egregious way in which the IP metaphor has distorted our thinking about human functioning. Whereas computers do store exact copies of data – copies that can persist unchanged for long periods of time, even if the power has been turned off – the brain maintains our intellect only as long as it remains alive. There is no on-off switch. Either the brain keeps functioning, or we disappear. What’s more, as the neurobiologist Steven Rose pointed out in The Future of the Brain (2005), a snapshot of the brain’s current state might also be meaningless unless we knew the entire life history of that brain’s owner – perhaps even about the social context in which he or she was raised.

'Multi-dimensional universe' in brain networks: Using mathematics in a novel way in neuroscience, scientists demonstrate that the brain operates on many dimensions, not just the 3 dimensions that we are accustomed to -- ScienceDaily

Using algebraic topology in a way that it has never been used before in neuroscience, a team from the Blue Brain Project has uncovered a universe of multi-dimensional geometrical structures and spaces within the networks of the brain.
The research, published today in Frontiers in Computational Neuroscience, shows that these structures arise when a group of neurons forms a clique: each neuron connects to every other neuron in the group in a very specific way that generates a precise geometric object. The more neurons there are in a clique, the higher the dimension of the geometric object.
"We found a world that we had never imagined," says neuroscientist Henry Markram, director of Blue Brain Project and professor at the EPFL in Lausanne, Switzerland, "there are tens of millions of these objects even in a small speck of the brain, up through seven dimensions. In some networks, we even found structures with up to eleven dimensions."
Markram suggests this may explain why it has been so hard to understand the brain. "The mathematics usually applied to study networks cannot detect the high-dimensional structures and spaces that we now see clearly."

The team found that individual ants had different yet consistent preferences. Some of the ants were happy to feed on either of the two solutions. Picky ants refused to feed from either. A third "middle" group consistently chose the solution with a higher concentration. These varied choices demonstrated that individual ants had individual thresholds to the sucrose concentration and made yes/no binary decisions accordingly.
The researchers then fed each colony again with the differing sucrose solutions and found that the majority of the ants in all six experimental colonies chose the 4.0% sucrose solution, without being influenced by other ants in the colony. The "collective" decision of the colony was thus for the more nourishing solution.
"Importantly, neither ants with a low threshold and high threshold contributed to the collective decision making, since the former didn't care about the concentration and the latter refused both concentrations. Thus, the decision maker was the middle group which preferred the higher concentration," says Hasegawa.
"The study demonstrates simple yes/no judgements by individuals can lead to a collective rational decision, without using quality-graded responses, when they have diverse thresholds in the population," he continued. This mechanism can be applied to various fields including brain science, behavioural science, swarm robotics and consensus decision-making in human societies, conclude the researchers.

What Is This Thing Called Consciousness?

Yet the cerebellum has everything you expect of neurons. It has gorgeous neurons. In fact, some of the most beautiful neurons in the brain, so-called Purkinje cells, are found in the cerebellum. Why does the cerebellum not contribute to consciousness? It has a very repetitive and monotonous circuitry. It has 69 billion neurons, but they have simple feed-forward loops. So I believe the way the cerebellum is wired up does not give rise to consciousness. Yet another part of the brain, the cerebral cortex, seems to be wired up in a much more complicated way. We know it’s really the cortex that gives rise to conscious experience.

Bipolar disorder: New method predicts who will respond to lithium therapy -- ScienceDaily

Wondering whether the differences could be predictive, the team trained a computer program to recognize the variations between the profiles of responders and nonresponders using the firing patterns of 450 total neurons over six independent training rounds. In each round, they started fresh with the neurons of five of the patients to train the system. They then tested the system with the neurons of the sixth patient, whose lithium status was known to the team but not to the program. They repeated the process five more times, which allowed them to build essentially six independent models. Each model was trained on the data from five out of the six patients, leaving a different patient out of the training data each time, and then letting the model classify this remaining patient as a responder or nonresponder. Using the firing patterns of just five of any patient's neurons, the system identified the person as a responder or nonresponder with 92 percent accuracy.

Mouse study identifies new method for treating depression: Inhibiting brain enzyme alleviates depression, and does it much faster than conventional antidepressants -- ScienceDaily

Palmer and team unraveled a previously underappreciated molecular process that can influence mouse models of depression. Here's how the process works: Cells generate energy. In doing so, they produce a byproduct. That byproduct inhibits neurons and thus influences various behaviors. Typically, the enzyme GLO1 removes this byproduct, but inhibiting GLO1 can also increase the activity of certain neurons in a beneficial way. In mice, Palmer and others have shown that more GLO1 activity makes mice more anxious, but less was known about the system's effect on depression.
Palmer and team wondered if they could reduce signs of depression by inhibiting the GLO1 enzyme.
The researchers used several different antidepressant tests. They compared responses in three groups of mice: 1) untreated, 2) treated by inhibiting GLO1, either genetically or with an experimental compound, and 3) treated with Prozac, a selective serotonin reuptake inhibitor commonly used to treat depression.
The first tests they used were the tail suspension test and the forced swim tests, which are often used to determine whether or not a compound is an antidepressant. In this case, the answer was yes. The other tests -- chronic forced swim test, chronic mild stress paradigm and olfactory bulbectomy -- are well-established measures that can also be used to measure how long it takes for an antidepressant to take effect.
In each of these tests, inhibiting the GLO1 enzyme reduced depression-like symptoms in five days, whereas it took 14 days for Prozac to have the same effect.
While this new approach to treating depression has so far only been tested in mice and it will take many years of development before a GLO1 inhibitor could be tested in humans, the researchers are excited to find that new, unexplored approaches to treating depression are out there.

Dopamine toggling governs decision making

The voltammetry results showed that fluctuations in brain dopamine level were tightly associated with the animal's decision. The scientists were actually able to accurately predict the animal's upcoming choice of lever based on dopamine concentration alone.
Interestingly, other mice that got a treat by pressing either lever (so removing the element of choice) experienced a dopamine increase as trials got under way, but in contrast their levels remained above baseline (didn't fluctuate below baseline) the entire time, indicating dopamine's evolving role when a choice is involved.
"We are very excited by these findings because they indicate that dopamine could also be involved in ongoing decision, beyond its well-known role in learning," adds the paper's co-first author, Christopher Howard, a Salk research collaborator.
To verify that dopamine level caused the choice change, rather than just being associated with it, the team used genetic engineering and molecular tools -- including activating or inhibiting neurons with light in a technique called optogenetics -- to manipulate the animals' brain dopamine levels in real time. They found they were able to bidirectionally switch mice from one choice of lever to the other by increasing or decreasing dopamine levels.
Jin says these results suggest that dynamically changing dopamine levels are associated with the ongoing selection of actions. "We think that if we could restore the appropriate dopamine dynamics -- in Parkinson's disease, OCD and drug addiction -- people might have better control of their behavior. This is an important step in understanding how to accomplish that."

How the brain maintains useful memories -- ScienceDaily

there are specific groups of neurons in the medial prefrontal cortex (mPFC) of a rat's brain -- the region most associated with long-term memory. These neurons develop codes to help store relevant, general information from multiple experiences while, over time, losing the more irrelevant, minor details unique to each experience.
The findings provide new insight into how the brain collects and stores useful knowledge about the world that can be adapted and applied to new experiences.
"Memories of recent experiences are rich in incidental detail but, with time, the brain is thought to extract important information that is common across various past experiences," says Kaori Takehara-Nishiuchi, senior author and Associate Professor of Psychology at the University of Toronto. "We predicted that groups of neurons in the mPFC build representations of this information over the period when long-term memory consolidation is known to take place, and that this information has a larger representation in the brain than the smaller details."

The Serotonin Surprise | DiscoverMagazine.com

Glenmullen has long suspected that drugs that alter serotonin metabolism cause profound changes in the brain. He bases his suspicion on a body of research during the last 20 years by scientists investigating another class of drugs that includes MDMA (Ecstasy) as well as fenfluramine, the diet drug recently removed from the market because of its association with heart valve problems. These drugs do more than just block serotonin reuptake; they primarily stimulate the release of large quantities of serotonin from nerve endings into the brain. The resulting flood is thought to cause the mind-altering effects of MDMA. And that flood, some scientists argue, leaves brain damage in its wake. When monkeys and rats are given high doses of serotonin releasers--up to 40 times the dose that people generally take--the microscopic architecture of their brains looks different from normal brains. The nerve fibers (axons) that carry serotonin to the target cells seem to change their shape and diminish in number--effects some scientists claim are properly understood as brain damage.

How aerobic exercise enhances neuroplasticity in the brain

A brief but intense period of aerobic exercise immediately reduces GABA, the main inhibitory neurotransmitter in the brain. GABA play an important role in regulating the brain’s capacity to undergo change or neuroplasticity. We observed reduced excitability of GABA-mediated networks in the motor cortex, which may explain findings from previous studies where enhanced neuroplasticity is observed after aerobic exercise.
Our findings may have implications for individuals after stroke, where GABA is a promising target for promoting neuroplasticity to promote recovery of motor function.

Synapses shrink 20% every night?!

The team deliberately did not know whether they were analyzing the brain cells of a well-rested mouse or one that had been awake. When they finally "broke the code" and correlated the measurements with the amount of sleep the mice had during the six to eight hours before the image was taken, they found that a few hours of sleep led on average to an 18 percent decrease in the size of the synapses. These changes occurred in both areas of the cerebral cortex and were proportional to the size of the synapses.
The scaling occurred in about 80 percent of the synapses but spared the largest ones, which may be associated with the most stable memory traces.

Talking therapy changes the brain's wiring, study reveals for first time -- ScienceDaily

CBT -- a specific type of talking therapy -- involves people changing the way they think about and respond to their thoughts and experiences. For individuals experiencing psychotic symptoms, common in schizophrenia and a number of other psychiatric disorders, the therapy involves learning to think differently about unusual experiences, such as distressing beliefs that others are out to get them. CBT also involves developing strategies to reduce distress and improve wellbeing.
The findings, published in the journal Translational Psychiatry, follow the same researchers' previous work which showed that people with psychosis who received CBT displayed strengthened connections between key regions of the brain involved in processing social threat accurately.
The new results show for the first time that these changes continue to have an impact years later on people's long-term recovery.

Cardiovascular fitness is thought to offset declines in cognitive performance, but little is known about the cortical mechanisms that underlie these changes in humans. Research using animal models shows that aerobic training increases cortical capillary supplies, the number of synaptic connections, and the development of new neurons. The end result is a brain that is more efficient, plastic, and adaptive, which translates into better performance in aging animals. Here, in two separate experiments, we demonstrate for the first time to our knowledge, in humans that increases in cardiovascular fitness results in increased functioning of key aspects of the attentional network of the brain during a cognitively challenging task. Specifically, highly fit (Study 1) or aerobically trained (Study 2) persons show greater task-related activity in regions of the prefrontal and parietal cortices that are involved in spatial selection and inhibitory functioning, when compared with low-fit (Study 1) or nonaerobic control (Study 2) participants. Additionally, in both studies there exist groupwise differences in activation of the anterior cingulate cortex, which is thought to monitor for conflict in the attentional system, and signal the need for adaptation in the attentional network. These data suggest that increased cardiovascular fitness can affect improvements in the plasticity of the aging human brain, and may serve to reduce both biological and cognitive senescence in humans.

Running + challenges lead to neurogenisis

Voluntary physical exercise (wheel running, RUN) and environmental enrichment both stimulate adult hippocampal neurogenesis but do so by different mechanisms. RUN induces precursor cell proliferation, whereas ENR exerts a survival-promoting effect on newborn cells. In addition, continued RUN prevented the physiologically occurring age-related decline in precursor cell in the dentate gyrus but did not lead to a corresponding increase in net neurogenesis. We hypothesized that in the absence of appropriate cognitive stimuli the potential for neurogenesis could not be realized but that an increased potential by proliferating precursor cells due to RUN could actually lead to more adult neurogenesis if an appropriate survival-promoting stimulus follows the exercise. We thus asked whether a sequential combination of RUN and ENR (RUNENR) would show additive effects that are distinct from the application of either paradigm alone. We found that the effects of 10 days of RUN followed by 35 days of ENR were additive in that the combined stimulation yielded an approximately 30% greater increase in new neurons than either stimulus alone, which also increased neurogenesis.

Self-generated vision inputs suppressed

That's because the brain can tell if visual motion is self-generated, canceling out information that would otherwise make us feel -- and act -- as if the world was whirling around us. It's an astonishing bit of neural computation -- one that Maimon and his team are attempting to decode in fruit flies. And the results of their most recent investigations, published in Cell on January 5, provide fresh insights into how the brain processes visual information to control behavior.
Each time you shift your gaze (and you do so several times a second), the brain sends a command to the eyes to move. But a copy of that command is issued internally to the brain's own visual system, as well.
This allows the brain to predict that it is about to receive a flood of visual information resulting from the body's own movement -- and to compensate for it by suppressing or enhancing the activity of particular neurons.

Experience-dependent reorganisation of functional maps in the cerebral cortex is well described in the primary sensory cortices. However, there is relatively little evidence for such cortical reorganisation over the short-term. Using human somatosensory cortex as a model, we investigated the effects of a 24-hour gluing manipulation in which the right index and right middle fingers (digits 2 & 3) were adjoined with surgical glue. Somatotopic representations, assessed with two 7 tesla fMRI protocols, revealed rapid off-target reorganisation in the non-manipulated fingers following gluing, with the representation of the ring finger (digit 4) shifted towards the little finger (digit 5) and away from the middle finger (digit 3). These shifts were also evident in two behavioural tasks conducted in an independent cohort, showing reduced sensitivity for discriminating the temporal order of stimuli to the ring and little fingers, and increased substitution errors across this pair on a speeded reaction time task.

Runners' brains may be more connected, research shows | EurekAlert! Science News

University of Arizona researchers compared brain scans of young adult cross country runners to young adults who don't engage in regular physical activity. The runners, overall, showed greater functional connectivity -- or connections between distinct brain regions -- within several areas of the brain, including the frontal cortex, which is important for cognitive functions such as planning, decision-making and the ability to switch attention between tasks.

How hearing loss can change the way nerve cells are wired -- ScienceDaily

In mice whose ears were blocked, cells in the auditory nerve started to use their supplies of neurotransmitter more freely. They depleted their reserves of these chemicals rapidly each time a new auditory signal came in, and they decreased the amount of space within the cells that housed sac-like structures called vesicles -- biological storage tanks where neurotransmitter chemicals are kept.
"When it's quiet, the demands on the auditory nerve cells are not as great," Xu-Friedman says. "So it makes sense that you would see these changes: You no longer need as much neurotransmitter, so why invest in a lot of storage? If you're not that active, you don't need a big gas tank. And you're not as afraid to use up what you have. This is one plausible explanation for what we observed."
The changes in cellular structure and behavior were the opposite of what Xu-Friedman team's saw in a previous study that placed mice in a consistently noisy environment. In that project -- faced with an unusually high level of noise -- the mice's auditory nerve cells started to economize their resources, conserving supplies of neurotransmitter while increasing the storage capacity for the chemicals.
"It looks like these effects are two sides of the same coin, and they might be the first hints of a general rule that nerve cells regulate their connections based on how active they are," Xu-Friedman says.

In order to elucidate these effects, researchers from the D'Or Institute for Research and Education (IDOR) and the Institute of Biomedical Sciences at the Federal University of Rio de Janeiro (ICB-UFRJ) exposed human neural progenitors to this beta-carboline. After four days, harmine led to a 70% increase in proliferation of human neural progenitor cells.
Researchers were also able to identify how the human neural cells respond to harmine. The described effect involves the inhibition of DYRK1A, which is located on chromosome 21 and is over activated in patients with Down syndrome and Alzheimer's Disease.
"Our results demonstrate that harmine is able to generate new human neural cells, similarly to the effects of classical antidepressant drugs, which frequently are followed by diverse side effects. Moreover, the observation that harmine inhibits DYRK1A in neural cells allows us to speculate about future studies to test its potential therapeutic role over cognitive deficits observed in Down syndrome and neurodegenerative diseases," suggests Stevens Rehen, researcher from IDOR and ICB-UFRJ.